Polychlorodibenzodioxin and -furan and Dioxin-like

Jun 21, 2013 - Polychlorodibenzodioxin and -furan and Dioxin-like Polychlorobiphenyl Distribution in Tissues and Dairy Products of Dairy Buffaloes ...
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Polychlorodibenzodioxin and -furan and Dioxin-like Polychlorobiphenyl Distribution in Tissues and Dairy Products of Dairy Buffaloes Stefania Paola De Filippis,*,† Claudia Chirollo,‡ Gianfranco Brambilla,† Aniello Anastasio,‡ Paolo Sarnelli,§ Elena De Felip,† Alessandro di Domenico,† Anna Laura Iamiceli,† and Maria Luisa Cortesi‡ †

Environment Department, Istituto Superiore di Sanità, Viale Regina Elena 299, I-00161 Rome, Italy Department of Veterinary Medicine and Animal Production, University of Naples Federico II, Via F. Delpino, 1, I-80137 Naples, Italy § Campania Region, Regional Veterinary Services, Centro Direzionale di Napoli, Isola C3, I-80141 Naples, Italy ‡

S Supporting Information *

ABSTRACT: A pilot study was performed on three different dairy buffalo herds exposed without exposure control conditions to Polychlorodibenzodioxins and -furans (PCDDs, PCDFs) and Dioxin-like Polychlorobiphenyls (DL-PCBs). This study dealt with the relationship between the contamination levels (pg WHO2005-TE/g fat) in individual raw milk and those in edible tissues and with the contamination transfer from farm bulk milk to dairy products. On a cumulative basis, kidney (41, 67, and 21 pg WHOTE/g fat) resulted more in equilibrium with milk (48, 42, and 20) than did muscle (25, 31, and 9), while liver showed a large bioaccumulation (221, 304, and 75), with marked differences of the congener profile. Mozzarella cheese contamination (23, 42, and 29 pg WHO-TE/g fat) was higher than that of bulk milk (20, 36, and 21), which suggested a role of casein precipitation in congener transfer. The above information could improve the effectiveness of risk management during a “dioxin” crisis. KEYWORDS: dioxins, buffaloes, milk, dairy products, meat, liver, fat, food safety, food security



INTRODUCTION During 2008, the dairy production system in Italy suffered from a “dioxins crisis” for noncompliance with the maximum levels of PCDDs, PCDFs, and DL-PCBs prescribed1 in buffalo dairy products. Even if confined to clustered areas within the Campania Region, and with a limited percentage of noncompliant results,2 the crisis had a strong impact on economics and social infrastructure, mainly related to the perception of quality associated with Mediterranean production systems and dietary habits. During such a crisis, extensive investigations were focused on the source(s) of contamination, which involved analyses on agricultural soils and farm forages and the follow-up of noncompliances in buffalo milk farms.3,4 It is now acknowledged that the PCDD, PCDF, and DL-PCB fallouts from occasional sources of contamination in corn and pasture determined the prolonged uptake of the aforementioned contaminants through locally produced forages, such as silages and grass hays, thus enabling the transfer of the environmental contaminant to the food of animal origin.5 In the risk management of this crisis, the following knowledge gaps were highlighted concerning the distribution of the aforementioned contaminants in animal tissues and dairy products: (a) the correlation between the contamination in milk and that in edible tissues, including liver, considering milk as a matrix suitable to predict the compliance of the carcass; (b) the correlation between the contamination in milk and that in dairy products (mozzarella cheese, whey, and whey cheese). These data were mandatory to grasp how the native milk contamination could affect the different dairy products and how © XXXX American Chemical Society

the possible mitigation or enhancement effects could impact the compliance of the food. Previous studies carried out mainly in long-term-exposed meat-producing animals (steady state) highlighted a possible correlation between WHO-TE levels and congener patterns in well-perfused organs, such as metabolic and muscle fat, thus suggesting the use of small biopsies as a noninvasive sampling procedure able to predict meat safety compliance.6 However, such studies may not be directly applicable to dairy animals, due to the changes of lipid metabolism associated with the energy balance during lactation, especially in the 90-day period after calving. Such changes could in fact alter the profile of the congeners and the related WHOTE level of the contamination.7 Schultz et al.8 reported PCDD, PCDF, and DL-PCB concentrations in muscles of dairy animals lower than those found in milk. The presence of an efficient clearance of lipophilic contaminants via milk may influence the concentration of the aforesaid contaminants in the different edible parts of the carcass (in a dairy buffalo, on average 1 kg of fat is excreted daily with milk). This point is of considerable importance, because the present European Union legislation sets the cumulative WHO-TE values on a lipid base in edible tissues and milk from food-producing terrestrial animals.9 In the scientific literature, more attention has been paid to report the occurrence of PCDDs, PCDFs, DL-PCBs, and other Received: March 5, 2013 Revised: June 6, 2013 Accepted: June 7, 2013

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dx.doi.org/10.1021/jf401004c | J. Agric. Food Chem. XXXX, XXX, XXX−XXX

Journal of Agricultural and Food Chemistry

Article

Table 1. Analytical (pg/g fat) and Cumulative (WHO2005-TE/g fat) Contamination Recorded in Milk, Muscle, Perirenal Fat (K), Retrobulbar Fat (E), and Liver from Three Dairy Buffaloes (A, B, and C)a farm A

congener, % fat 2,3,7,8-TCDD 1,2,3,7,8-PeCDD 1,2,3,4,7,8-HxCDD 1,2,3,6,7,8-HxCDD 1,2,3,7,8,9-HxCDD 1,2,3,4,6,7,8HpCDD OCDD total PCDDs UB 2,3,7,8-TCDF 1,2,3,7,8-PeCDF 2,3,4,7,8-PeCDF 1,2,3,4,7,8-HxCDF 1,2,3,6,7,8-HxCDF 1,2,3,7,8,9-HxCDF 2,3,4,6,7,8-HxCDF 1,2,3,4,6,7,8HpCDF 1,2,3,4,7,8,9HpCDF octaCDF total PCDFs UB PCB 77 PCB 81 PCB 126 PCB 169 total non-orthoPCBs UB PCB 105 PCB 114 PCB 118 PCB 123 PCB 156 PCB 157 PCB 167 PCB 189 total mono-orthoPCBs UB total PCDDs + PCDFs UB total DL-PCBs UB cumulative UB a

farm B

farm C

milk

muscle

K fat

E fat

liver

milk

muscle

K fat

E fat

liver

milk

muscle

K fat

E fat

liver

25.6 3.15 9.79 4.22 33.2 5.16 13.9

1.50 2.42 5.76 1.99 13.3 1.61 7.50

N.A.b 3.07 9.90 3.16 29.1 3.73 15.4

N.A. 2.16 5.43 1.53 8.80 1.04 2.80

3.42 4.15 36.4 47.4 96.2 24.9 262

9.27 6.15 10.6 2.15 16.0 2.13 5.71

1.55 5.12 7.90 2.42 12.7 1.44 7.75

N.A. 7.78 17.0 5.34 46.1 4.83 28.5

N.A. 8.45 13.5 2.67 18.7 2.58 4.89

4.60 10.9 61.7 69.7 122 34.7 412.7

10.9 2.05 3.74 0.79 3.78 0.89 2.18

1.30 1.06 1.48 0.52 1.80 0.43 1.83

N.A. 2.21 4.20 1.32